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Using a selective ARC-deficient POMC mouse line, here we report that former obesity medications augmenting endogenous 5-hydroxytryptamine (5-HT) activity d-fenfluramine and sibutramine require ARC POMC neurons to elicit therapeutic appetite-suppressive effects.
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The development of the Nf1 GRD/+ mouse line described here will allow researchers to determine the necessity of GRD function across the spectrum of developmental and tumor phenotypes observed in mouse models of neurofibromatosis.
The R26PR mouse line described here is a powerful model for the spatial and temporal control of Prdm14 misexpression, which can be used to investigate the role of PRDM14 in multiple cancer types.
The two new mouse lines described here expand the repertoire of genetically engineered mice available for controlled in vivo recombination and cell labeling using the Cre-lox system.
In other mutant mouse lines referenced here [23], [30], [34], [35], [36], the responsible genes encode Wnt antagonists that repress Wnt transcription or the Wnt response.
The new mutant mouse lines described here were used to address the following questions: i) is PiT1 essential for embryo development?
The two new mouse lines described here add to the growing list of genetically engineered mice available for controlled in vivo recombination and cell labeling using the Cre-lox system.
Inbred lean (Lean) and fat (Fat) mouse lines used here were developed by long-term (over 60 generations) divergent selection for low or high body fat % [ 9, 16].
Since all three Crb1 rd8/rd8 mouse lines studied here were raised in the same environment, but still showed prominent differences in their phenotype, predominantly genetic factors may define these additional phenotypic features.
Notably, screening of available data from Jackson Laboratories (http://www.jaxlab.org) revealed that the two mouse lines employed here are not polymorphic for the Mecp2 3′UTR allele or the miR-511 sequence.
This new mouse line and experimental regimes described here should be useful in studying coronary vessel behavior during postnatal growth and in the adult during injury, regeneration, and diseases.
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